This document discusses the analysis of HRCT scans in diffuse lung diseases. It begins by describing the anatomy of the secondary pulmonary lobule and the distribution patterns seen in different lung diseases. Centrilobular, lymphatic, and random distributions are described. Common diseases are then discussed in more detail, including their typical imaging findings and distributions. These include sarcoidosis, pulmonary edema, lymphangitic spread of tumors, and various interstitial lung diseases. The role of HRCT in evaluating features like ground glass opacities, nodules, septal thickening, and honeycombing is emphasized to differentiate between conditions and guide diagnosis.

1. HRCT chest in diffuse lung
diseases
Dr Subash Pathak
Resident, MD Radiodiagnosis
NAMS

2. Secondary Pulmonary Lobule
• The secondary lobule - the basic anatomic unit of pulmonary structure and
function.
• Smallest lung unit that is surrounded by connective tissue septa.
• Interpretation of interstitial lung diseases is based on the type of
involvement of the secondary lobule.
• Supplied by a small bronchiole or terminal bronchiole in the center,
parallelled by the centrilobular artery.
• The pulmonary veins and lymphatics run in the periphery of the lobule
within the interlobular septa.
• Measures 1-2 cm, 5-15 pulmonary acini, containing alveoli for gas
exchange.

3. • Centrilobular area -
Central part of the secondary lobule.
Site of diseases, that enter the lung through the airways ( i.e.
hypersensitivity pneumonitis, respiratory bronchiolitis, centrilobular
emphysema ).
• Perilymphatic area
 Peripheral part of the secondary lobule.
 Site of diseases located in the lymphatics of in the interlobular septa ( i.e.
sarcoid, lymphangitic carcinomatosis, pulmonary edema).

4. Centrilobular area in blue and perilymphatic
area in yellow.
Secondary lobules. The centrilobular artery (in blue: oxygen-
poor blood) and the terminal bronchiole run in the centre.
Lymphatics and veins (in red: oxygen-rich blood) run within the
interlobular septa

5. Practical approach in diagnosing diffuse lung
disease in HRCT
• Analysis of distribution of the abnormalities
• Interpretation of pattern in relation to distribution
• Utilisation of associated imaging findings and clinical information
• Chronicity of the findings

6. Diffuse lung disease: Present or absent!
• First step is to
determine the presence
of diffuse lung disease
• Dependent
density/Atelectasis
need to be
differentiated
• May need additional
imaging in prone
position.
Figure 2. Diffuse lung disease: present or not present A. Supine high-resolution
CT image of the lung shows faint opacities in the dependent portion of the
lung, requiring differentiation between diffuse lung disease versus dependent
opacities. B. On a prone high-resolution CT image at a similar level, the
dependent opacities persist, indicating that the opacities are not gravity-
dependent, and confirms the presence of diffuse lung disease

7. Distribution of the abnormalities
• Upper, middle and lower lung distribution
• Peripheral or central
• Distribution in relation to secondary pulmonary lobule i.e. Lymphatic,
centrilobular, and random

8. Upper, middle and lower lung distribution
• Lung is divided into 3 areas in cranio-caudal directions.
• Predisposition of upper lungs: Sarcoidosis, Hypersensitivity
pneumonitis, Silicosis
• Lower lungs predisposition: Idiopathic pulmonary fibrosis (IPF), NSIP.

9. Peripheral or central distribution
• Peripheral lung: 2-3 rows of secondary pulmonary lobules forming a
layer of 3-4 cm thickness at lung periphery and along the lung
surfaces adjacent to fissures
• Central lung: remaining lung
• Peripheral distribution: Cryptogenic organising pneumonia (COP), IPF
• Central distribution: Cardiogenic pulmonary edema or alveolar
proteinosis
• Subpleural distribution: IPF/NSIP (subpleural areas of lungs and
extend along pleura and fissures)

10. Distribution in relation to secondary
pulmonary lobule
Secondary pulmonary lobule A. Radiograph of 1-mm thick section of lung specimen demonstrates a
polygonal structure composed of several acini conducted by terminal bronchioles, representing a secondary
pulmonary lobule. B. Radiograph of 1-mm thick section of lung specimen shows interlobular septum
(arrowheads) which defines the boundary of the secondary pulmonary lobule and the bronchovascular
bundles (arrows), which run into the center of the secondary pulmonary lobule.

12. Lymphatic distribution
• Lymphatic system is present along both
the bronchovascular bundles and
interlobular septum.
• Disease of the lymphatic system involves
both.
• Major and minor fissure involvement.
• Pulmonary edema, sarcoidosis,
lymphangitic spread of tumor or
lymphoma.
Lymphatic distribution: Lymphangitic spread of tumor Coronal
CT images of a patient with lymphangitic spread of colon
cancer demonstrate the thickening of both interlobular septum
(arrowheads) and bronchovascular bundles (arrow).

13. Centrilobular distribution
• Small airway related diseases
• Sparing of the interlobular septa unless the disease process fills the
whole of secondary pulmonary lobule.
• In many cases, centrilobular nodules are ground glass attenuation and
are ill defined.
Causes:
Hypersensitivity pneumonitis
Respiratory bronchiolitis in smokers
Infectious airways diseases (endobronchial spread of tuberculosis or
nontuberculous mycobacteria, bronchopneumonia)
Uncommon in bronchioloalveolar carcinoma, pulmonary edema, vasculitis

14. Ill defined centrilobular nodules of
ground glass density in a patient with
hypersensitivity pneumonitis
Centrilobular distribution: Tuberculosis High-resolution CT
image of a patient with tuberculosis demonstrates ill-defined
nodular opacities along the bronchovascular bundles, sparing
the interlobular septum.

15. Random distribution
• Distribution has no relation to secondary pulmonary lobule.
• Seen in:
Miliary tuberculosis
Hematogeneous metastases
Disseminated fungal infections
Sarcoidosis (usually perilymphatic distribution).However, when very
extensive, it spreads along the lymphatics in the bronchovascular bundle to
the periphery of the lung and may reach the centrilobular area.
This may result in a combined perilymphatic-centrilobular pattern which
can simulate the random pattern.
Langerhans cell histiocytosis (early nodular stage)

16. Random distribution of nodules in
miliary tuberculosis
Langerhans cell histiocytosis: early nodular
stage before the typical cysts appear.

17. Could this be UIP or NSIP?
• Two most common forms of idiopathic interstitial lung disease.
• Both have peripheral and basilar distribution often with decreased
lung volumes.

18. Usual Interstitial Pneumonia
• Histopathological abnormality
• Hallmark of heterogeneous appearance with alternating areas of normal
lung, interstitial inflammation, fibrosis and honeycombing.
• Subpleural peripheral parenchyma most severely affected.
• Characteristics HRCT findings:
Peripheral and basilar distribution
Honeycombing
Decreased lung volume unless associated with emphysema
Traction bronchiectasis, interlobular septal thickening and GGO may be
present

19. • Honeycombing: Clustered cystic air
spaces (average size 0.3-1 cm) with
clearly defined 1-3 mm thick walls,
predominantly peripheral and
subpleural distribution.
• Subpleural honeycomb cysts typically
occur in several contiguous layers.
(Differentiates from paraseptal
emphysema where cysts are in a single
layer)
• Represent end stage fibrotic lung
disease.
• UIP: Histologic diagnosis, lung reacton
pattern to injury.
• If idiopathic, called IPF.
• Secondary: Exposure to dusts eg
asbestosis, Drugs eg Bleomycin,
Collagen vascular disease

20. Idiopathic pulmonary fibrosis A. High-resolution CT image
shows a diffuse lung disease with peripheral and basilar
distribution and honeycombing, indicating IPF/Collagen
vascular disease/asbestosis.
Honeycombing and traction bronchiectasis in UIP.

21. Differential Diagnosis
• Chronic hypersensitivity pneumonitis: Mosaic pattern with sparing of
lung bases or when there are centrilobular nodules.
• End stage sarcoidosis: Fibrosis in posterior part of upper lobes and in
perihilar area, nodules in perilymphatic distribution and extensive
mediastinal lymphadenopathy.
• NSIP

22. Nonspecific Interstitial Pneumonia (NSIP)
• Histologic entity, inflammation and fibrosis predominantly affecting
alveolar walls.
• Prevalent lung pattern in connective tissue diseases (Systemic
sclerosis, dermatomyositis, polymyositis, RA, SLE)
• HRCT:
Basal predominant GGO
Traction bronchiectasis
Lower lobe volume loss
No or only mild honeycombing

23. Non-specific interstitial pneumonia A, B. High-resolution CT images of a patient with
NSIP shows a diffuse lung disease with peripheral distribution, demonstrating ground
glass opacities, traction bronchiectasis/ bronchiolectasis, without definite
honeycombing

24. S.No. Features NSIP UIP
1. Age at presentation A decade earlier > 50 years
2. Sex distribution M:F F>M M>F
3. Presenting symptoms
(Progressive dyspnea, non
productive cough)
Milder More severe
4. HRCT findings:
Ground glass opacities
Honeycombing
Lung volume loss
Common
May be present, mild
Lower lobe
May
Dominant feature
Whole lung
5. Histology Homogeneous uniform
pattern of cellular
interstitial inflammation
associated with variable
degree of fibrosis
Extensive fibrosis
which is temporally
inhomogeneous i.e.
Various lesions are
of different ages
6. Response to steroid Yes No
7. Prognosis Good Bad

25. Interpretation of pattern in relation to
distribution
• After determining the distribution and ruling out UIP and NSIP, next
step is to determine pattern in relation to distribution.
• Diseases with same morphological pattern but with different
distributions have totally different diagnosis.
• In addition, associated imaging findings and clinical information also
needs to be considered to narrow down the differentials.
• Chronicity of the findings along with assessment of previous imaging
findings also helps.

26. Diseases of the lymphatic system
• Involvement of interlobular septum, fissures and pleura, along with
bronchovascular bundles: Thickening of these structures
• Thickenings can be smooth, irregular or beaded.
• Differentials:
Pulmonary edema
Sarcoidosis
Lymphangitic spread of tumor
Lymphoma

27. Pulmonary Edema
• Smooth interlobular septal
thickening
• Associated findings: diffuse ground
glass opacities, pleural effusion, and
cardiomegaly.
• Acute process, so need to assess for
chronicity of findings.
Pulmonary edema CT scan of a patient with dyspnea on
exertion demonstrate smooth interlobular septal thickening at
the lung bases (arrowheads), associated with left pleural
effusion, representing pulmonary edema

28. Sarcoidosis
Systemic disorder of unknown origin.
characterized by non-caseating granulomas in
multiple organs
May resolve spontaneously or progress to fibrosis.
Pulmonary manifestations are present in 90% of
patients.
Systemic symptoms such as fatigue, night sweats
and weight loss are common.

29. • Loefgren's syndrome, an acute presentation of sarcoidosis, consists of
arthritis, erythema nodosum, bilateral hilar adenopathy and occurs in 9-
34% of patients.
• Upper and middle lung distribution
• Beaded or irregular apperance with thickened bronchovascular bundles,
interlobular septum, fissure and pleura.
• Associated imaging findings: Symmetric and bilateral mediastinal and hilar
lymphadenopathy, architectural destruction due to chronic inflammation,
and extensive fibrosis in upper lung with volume loss.
• Clinical association: Uveitis, elevated ACE level.
• < 5% of patients die from end stage lung disease from pulmonary fibrosis/

30. Sarcoidosis stage I: left and right hilar and
paratracheal adenopathy (1-2-3 sign) Sarcoidosis: typical presentation with nodules along
the bronchovascular bundle and fthe issuresNotice the
partially calcified node in the left hilum.
Sarcoidosis with conglomerate
masses of fibrous tissue

31. Sarcoidosis High-resolution CT image demonstrates a
nodular thickening of bronchovascular bundles,
interlobular septum and fissures, representing
characteristic findings in pulmonary sarcoidosis
Sarcoidosis with fibrosis in the upper lobes.
Typical chest film.
Sarcoidosis with fibrosis in the upper lobes. Typical HRCT
findings.

32. Lymphangitic spread of tumor and lymphoma
• Typically lower lung distribution
• Can be asymmetric
• Associated imaging findings:
Lymphadenopathy in mediastinum,
axilla, supraclavicular, intraabdominal,
can be asymmetric and necrotic
• In contrast to sarcoidosis, architectural
distortion and extensive fibrosis not
usually present.

33. Lymphatic pattern: lymphangitic spread of tumor A, B. High-resolution CT images of the
lower lungs demonstrate irregular thickening of the interlobular septum and
bronchovascular bundles, representing a “lymphatic pattern” due to lymphangitic spread
of tumor.

34. Nodular Lung Disease
• Random Nodules
• Centrilobular nodules
• Nodules in lymphatic distribution

35. Random nodules
• Divided based on nodule sizes:
• Fine nodules: approximately 3 mm or
less
D/D: Miliary tuberculosis, metastases,
disseminated fungal infections.
• Medium or large size nodules: > 3 mm.
Metastases, tuberculosis and fungal
infections in immunocompromised.
Fine nodules: metastasis High-resolution CT image
demonstrates multiple fine discrete nodules in
random distribution, representing miliary
metastasis from thyroid cancer.

36. Centrilobular nodules
• Along bronchovascular bundles
• Infections or inflammations
• Neoplasms spreading along the
airway such as BAC, lymphoma
• Centrilobular nodules, ansence of
interlobular septal thickening.
• Centrilobular opacities in branching
pattern: Tree in bud appearance:
Dilated centrilobular bronchioles
impacted with mucus, fluid or pus.

37. Typical Tree-in-bud appearance in a patient with active TB.
Mycobacterium avium-intracellulare infection High-resolution
CT image of a 69-year-old male with productive cough and
hemoptysos demonstrates multiple branching opacities due to
impacted impacted centrilobular bronchioles representing
“tree-in-bud” appearance, associated with diffuse
bronchiectasis

38. Ground glass opacities
• Hazy increase in lung opacity not associated with obscuration of underlying
vessels
• Seen in many conditions with anything occupying alveoli, interstitium or
both.
• Common causes are:
Hypersensitivity pneumonitis
Diffuse infection such as pneumocystis jerovecii (PCP), CMV
Pulmonary edema
ARDS
Diffuse pulmonary hemorrhage

39. • Analysis of distribution helps in D/D
• Central GGO: Acute: Pulmonary edema, Chronic: Alveolar proteinosis
• Peripheral GGO: NSIP, COP and DIP
• Centrilobular GGO: Hypersensitivity pneumonitis and RB-ILD

40. Hypersensitivity pneumonitis
• A/K/A extrinsic allergic alveolitis (EAA)
• Causation: inhalation of a variety of antigens (farmer's lung, bird fancier's
lung, 'hot tub' lung, humidifier lung).
• Acute, subacute, and chronic stages.
• HRCT usually performed in subacute stage months after first exposure
• Subacute hypersensitivity pneumonitis: Key imaging findings:
Ill-defined centrilobular nodules of ground-glass opacity (80% of cases) or
mosaic pattern of a combination of patchy ground-glass opacity due to
lung infiltration and patchy lucency due to bronchiolitis with air trapping

41. case of hypersensitivity pneumonitis.There is a mosaic pattern.
Some secondary lobules demonstrate ground-glass opacity due
to lung infiltration, while others are more lucent due to
bronchiolitis with air trapping.
Subacute hypersensitivity pneumonitis with
ill-defined centrilobular nodules
subtle opacity in the centre of the secondary lobules (arrows)
with sparing of the subpleural region
subtle centrilobular opacity in a patient with subacute HP

42. Chronic hypersensitivity pneumonitis
The key findings in chronic
hypersensitivity pneumonitis are:
• Mosaic pattern with areas of ground-
glass attenuation and areas of low
attenuation.
• Fibrosis and parenchymal distortion in
a mid zone distribution. Chronic hypersensitivity pneumonitis: Nonspecific chest film,
typical HRCT-findings.
Mosaic pattern with hyperaerated secondary nodules and
secondry nodules of increased attenuation.
Additionally there is septal and intralobular reticular
thickening, indicating already existing irreversible fibrosis.

43. Differential diagnosis of Hypersensitivity
Pneumonitis.
• Subacute stage:
• RB-ILD: seen in smokers, upper lobe predilection, usually associated with
centrilobular emphysema.
• Alveolar proteinosis.
• Chronic stage:
• UIP: may show very similar HRCT findings.
UIP has a strong lower zone distribution.
In chronic HP fibrotic changes are typically seen throughout the whole lung
parenchyma from the periphery towards the centrum.

44. UIP with honeycombing (left) and chronic HP (right)

45. Diffuse infections including PCP and CMV
pneumonia
• Immunocompromised
patients with infectious
symptoms
• PCP: CD4 count <200
cells/mm3
Pneumocystis carinii pneumonia High-resolution CT image of
an HIV positive patient with fever demonstrates diffuse ground
glass opacities in bilateral lungs.

46. Pulmonary edema
• m/c diffuse lung disease with
ground glass attenuation
• GGO is centrally distributed with
smooth interlobular septal
thickening.
Pulmonary edema High-resolution CT image in a patient with
congestive heart failure shows diffuse groundglass opacities
with somewhat central distribution, sparing the subpleural
area.

47. ARDS
• Diffuse lung injury leading to permeability edema and diffuse alveolar
damage.
• Life threatening, patient often requires mechanical ventillation.
• Predisposing factors can be pulmonary or extrapulmonary.
• Extrapulmonary causes usually show symmetric distribution.
• HRCT: Diffuse/patchy GGO or consolidation, predominantly in
dependent lung portions.
• Mild forms resolve completely while severe forms end in irreversible
fibrosis.

48. patient who was involved in a traffic accident and
within hours developed ARDS.
The dominant pattern is ground glass opacity.
In the dependent parts of the lung there is also
some consolidation, so there is a gradient from
front to back. Extra-pulmonary ARDS with gravity
dependent gradient
patient who developed ARSD as a result of pneumonia (i.e.
pulmonary ARDS).Note the patchy distribution of lung disease
and the almost complete distorsion more basal.Pulmonary
ARDS with asymmetric patchy distribution of consolidations.

49. Diffuse Pulmonary Hemorrhage
• Patchy or diffuse GGO,
sometimes with consolidation
and ill defined centrilobular
opacities.
• Causes: Broad, Goodpasteur`s
syndrome, Vasculitis, collagen
vascular diseases,
coagulopathy, drug reactions
• Etiological identification is
difficult. Diffuse pulmonary hemorrhage A, B. High-resolution CT images in a 58-
year-old man with hemoptysis demonstrate diffuse ground glass
opacities throughout the lungs representing diffuse pulmonary
hemorrhage, with bilateral pleural effusion.

50. Pulmonary alveolar proteinosis
• Alveolar spaces are filed with PAS
positive lipid rich proteinaceous
material.
• Adults between 30 to 50 years.
• Non productive cough, fever and
mild dyspnea
• Crazy paving pattern: bilateral
GGO in patchy or geographic
distribution with smooth
interlobular septal thickening.

51. Smoking related diffuse lung disease
• RB-ILD
• DIP
• LCH

52. RB-ILD
• Clinicopathologic entity characterised by symptomatic interstitial lung
disease
• Associated pathologic lesions of respiratory bronchiolitis
• HRCT:
Centrilobular ground glass opacities
Thickening of central and peripheral airways with associated
centrilobular emphysema and air trapping.
Distribution: Predominant upper lobes

53. A smoker with RB-ILD with subtle HRCT-findings.
The dominant pattern is ground glass opacification.
Additional findings in this patient are paraseptal
emphysema in the upper lobes and some subtle
septal thickening in the basal parts.
Two different patients with similarl HRCT findings.
The left one is a smoker with RB-ILD and the patient
on the right has hypersensitivity pneumonits. Note
the difference in severity of ground glass opacities
and the well defined areas of airtrapping in HP.

54. DIP
• Idiopathic interstitial pneumonia
• Increased number of pigmented macrophages evenly dispersed
within alveolar spaces.
• Both RB-ILD and DIP affect cigarette smokers 30-40 years of age, M:F
of 2:1.
• PFT shows restrictive abnormality and decreased DLCO.
• Significant clinical, radiological and pathological overlap between
these two conditions reflecting different severity of small airways and
parenchymal reaction to cigarette smoking.
• DIP is considered the end spectrum of RB-ILD.

55. HRCT findings
• Ground glass opacity with peripheral and patchy or diffuse
distribution
• Occasional interlobular septal thickening
• Predominant lower lung distribution

56. Figure 21. Desquamative interstitial pneumonia A, B. High-resolution CT images of a 49-
year-old woman with history of heavy smoking show ground glass opacities with patchy
and somewhat peripheral distribution, as well as mild septal thickening

57. Pulmonary LCH
• Uncommon, destruction of distal airways by bronchocentric
granulomas containing Langerhans cells.
• Unknown etiology, young adults, associated with cigarette smoking.
• M=F
• Cysts and nodules in centrilobular distribution
• Upper and middle lung predominance sparing costophrenic angles
• Cyst walls are thin (may be thick), usually round shape can be bizzare,
usually less than 1 cm, can be larger.
• Combination of small nodules of varying sizes with indistinct margins.

58. LCH
• Cavitation of nodules often seen
with relatively thick wall
• Lung volumes usually normal or
increased
• Prognosis: Complete remission
after smoking cessation or
development of cystic lung
disease.
Figure 22. Pulmonary Langerhans cell histiocytosis High-
resolution CT image of a 28-year-old woman with history of
smoking shows cysts with nodular-appearing walls as well as
small cavitary nodules, predominantly in upper lung
distribution

59. Diffuse lung disease with increased lung
volume
• Lymphangioleiomyomatosis (LAM)
• Pulmonary LCH
• Emphysema with fibrosis

60. Lymphangioleiomyomatosis (LAM)
• Rare idiopathic disorder
• Diffuse interstitial proliferation of bundles of immature smooth
muscle cells in the wall of enlarged air cavities.
• Almost exclusively in females of child bearing age
• Dyspnea on exertion, occ pneumothorax, progressive loss of
pulmonary function
• Slowly progressive with eventual respiratory failure and death
• Antiestrogen therapy and lung transplantation.
• No relation to smoking

61. HRCT
• Multiple thin walled cysts
with diffuse and random
distribution, involvement
of costophrenic angles
• Ground glass opacities or
mild septal thickening
may be seen
• Increased lung volumes
• Recurrent pneumothorax
and pleural effusion.
Lymphangioleiomyomatosis A, B. High-resolution CT images of
a young female patient with LAM demonstrates multiple thin-
walled cystic changes associated with ground glass opacities
throughout the lung, including the costophrenic angle.

62. Emphysema with fibrosis
• Relatively common
• Emphysema predominates centrally in upper and middle lung areas
• Fibrosis predominates peripherally and in basal areas
• PFT may appear normal due to obstructive change due to
emphysema and restrictive change due to fibrosis.

63. Bilateral multiple parenchymal opacities
• Multiple areas of increased lung attenuation, usually less round than
nodules
• Many differentials including infections, neoplasms, vasculitis or other
inflammatory pathologies.
• Distribution pattern is important.
• Example: Peripheral distribution: COP, CEP, thromboembolic disease
• Associated clinical information is also important.
• Infections and neoplasms need to be considered first, then interstitial
lung disease and vasculitis, and then thromboembolic disease.

64. Infections
• Bacterial or fungal infections
• Important etiologies: Invasive aspergillosis,
cryptococcosis, coccidiodomycosis, and
nocardiosis
• Immunocompromised patients
• Invasive aspergillosis: Ill defined nodular or
consolidative opacities with surrounding
GOOs in early phase (Halo sign), Cavitary
nodules with air crescent due to necrosis
in late phase.
• Common in neutropenic patients with
immunosuppression,
Invasive aspergillosis High-resolution CT image
of a 54-year-old man with myelodysplastic
syndrome, neutropenia and fever,
demonstrates multiple ill-defined nodular
opacities surrounded by ground glass
opacities, and consolidations with air-
bronchogram.

65. Neoplasm
• Bronchioalveolar cell carcinoma
• Lymphoma
• Lymphoproliferative disorders
• Differentiation is difficult
• Indistinguishable from pneumonia
• So needs correlation with clinical
symptoms and observation of
chronicity and chronological changes.
Bronchioalveolar cell carcinoma High-resolution CT
image of a patient with bronchioalveolar cell
carcinoma demonstrate multiple parenchymal
opacities in both lungs. Differentiation between
other neoplastic or infectious processes is difficult
based on imaging findings alone.

66. Cryptogenic Organising Pneumonia (COP)
• Organising pneumonia of idiopathic cause
• Cough, dyspnea, malaise, fever, and weight loss
• Granulation tissue within bronchiolar lumen and
alveolar duct on histology
• Inflammatory process in which the healing
process is characterised by organisation of
exudates rather than resorption.
• Mostly idiopathic, may be seen in pulmonary
infections, drug reactions, collagen vascular
disease, WG, toxic fume inhalation.
• Steroid treatment, good prognosis
Cryptogenic organizing pneumonia High-resolution CT image
of a patient with recurrent pneumonia shows parenchymal
opacities with characteristically peripheral distribution in
bilateral lungs.

67. HRCT findings in COP
• Bilateral peripheral consolidations, sharply demarcated.
• Consolidations may be migratory.
• Lesions may show pleural tags or spiculae and give the impression of
volume loss and slight retraction of the surrounding parenchyma (DD
bronchogenic carcinoma).
• Bronchial wall thickening and dilatation are seen in most patients and
are usually restricted to areas of consolidation or ground glass
opacifications.
• Additional findings are pleural thickening, small pleural effusions and
parenchymal bands.

68. patient with the typical bilateral
peripheral consolidations of OP
patient with rheumatoid arthritis and bilateral
peripheral consolidations as a result of organizing
pneumonia.Patients with OP associated with
collagen vascular diseases respond less well to
therapy with steroids.
patient who complained of arthritic pain.
There are multiple small bilateral peripheral consolidations.
organizing pneumonia, related to collagen vascular disease.

69. Chronic Eosinophilic Pneumonia (CEP)
• Idiopathic, eosinophilic rich exudates in alveoli and interstitium
• History of allergic disease
• Cough with mucoid sputum, high fever, night sweats, lasting more than 3
months.
• Peripheral eosinophilia in 90% patients.
• CXR: Classically described as photographic negative of pulmonary edema
showing peripheral non-segmental homogeneous consolidation with or
without air bronchograms.
• HRCT: patchy bilateral parenchymal consolidation with peripheral and
upper lung distribution with associated ground glass opacities
• Linear or band like subpleural opacities may be seen.

70. 40 Y/M, 2-3 months of shortness of breath, fever, and
cough. No hemoptysis. CXR: Multiple regions of airspace
opacification are present throughout both lungs, most severe
in the left upper lobe. No pleural effusion. HRCT: Peripheral
areas of airspace consolidation throughout both lungs with a
predominance for the middle and upper lobs.
Blood: Peripheral blood eosinophilia
BAL: 71% eosinophils, negative for malignancy

71. Vasculitis
• Group of disorders causing inflammation and necrosis of blood
vessels
• Frequency and manifestations of lung involvement varies.
• Primary vasculitis presenting with bilateral multifocal parenchymal
opacities are:
• Wegeners granulomatosis
• Allergic angiitis and granulomatosis (Churg Strauss syndrome)

72. Wegener`s granulomatosis
• Necrotising granulomatous vasculitis of the respiratory tract,
segmental glomerulonephritis and small vessel vasculitis.
• 90% patients: Pulmonary involvement
• Sinusitis, cough, hemoptysis, hematuria
• cANCA positive
• HRCT: Bilateral multiple rounded opacities of varying sizes in random
distribution
• Cavitation is common, thick wall with irregular inner margin
• Consolidation and ggo associated with hemorrhage

73. Wegener’s granulomatosis High-resolution CT image of a 69-
year-old woman with cough and sinusitis demonstrates
multiple ill-defined opacities varying in size and appearance.

74. 34/F Cough and fever. Recurrence of symptoms three
months after her last hospitalization. CT scout: Large
bilateral pulmonary cavities, the largest ones containing liquid
forming fluid level. HRCT: Large bilateral pulmonary cavities,
the largest ones containing liquid forming fluid level. CT: Large
bilateral pulmonary cavities, the largest ones containing liquid
forming fluid level.

75. Allergic angiitis and granulomatosis (Churg-
Strauss syndrome)
• Generalized necrotising vasculitis, extravascular granuloma formation
and eosinophilic infiltration.
• Multisystem disorder, lungs are almost always involved
• Air space consolidation or GGO peripherally distributed
• Multiple nodular lesions of varying sizes
• Cavitation less than in Wegner`s
• Diffuse coarse reticulation can occur
• Imaging findings typically waxes and wanes
• History of asthma, nasal polyps and sinusitis.

76. 60 years/M: Past history of asthma and sinonasal polyps. Non-smoker. Known stables
pulmonary nodules without PET uptake for 3 years. Subacute dyspnea. Peripheral
eosinophilia on bloodwork.
Initial CT: Peripheral consolidation / ground
glass opacity and solid centrilobular nodules
(non cavitated).
3 months after antibiotic treatment: Persistent peripheral
consolidation / ground glass opacity and solid centrilobular
nodules (non cavitated), except the left part which
underwent slight changes with now a moderate pleural
effusion. There is no obvious migratory
consolidation/GGO.

79. References
• Radiology Assistant: Lung - HRCT Basic Interpretation and Lung -
HRCT Common diseases
• A Practical Approach to High-Resolution CT of Diffuse Lung
DiseaseMizuki Nishino, M.D.1,*, Harumi Itoh, M.D., Ph.D2, and
Hiroto Hatabu, M.D., Ph.D.3,*

81. THANK YOU